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Normal sexual function in males involves several discrete components: libido, initiating and maintaining erection, orgasm, ejaculation, and the refractory period. The penis is a vascular organ that exists in a continuum from the flaccid to the erect position. Erectile dysfunction is a condition that occurs when penile erection sufficient for vaginal penetration cannot be achieved by normal physiological means. Recent developments in basic science as well as clinical research have led to a better understanding of the physiological mechanisms regulating the erectile function of the penis. Anatomical studies have delineated the veno-occlusive mechanism of the corporal bodies, which is the critical mechanism of restricting blood outflow from the penis. Analysis of corporeal tissue and the use of animal models have further elucidated the mechanisms regulating corporeal smooth muscle tone (1-4).

Penile erection is a neurovascular event that occurs when blood flow to the penis exceeds flow out of the penis. Successful erections depend on precise modulation of neural pathways as well as penile vascular integrity (1,5-8). The relaxation oftrabecular smooth muscle results in increased blood flow to the corpora cavernosa, leading to sinusoidal

From: Current Clinical Urology: Male Sexual Function: A Guide to Clinical Management, Second Edition Edited by: J. J. Mulcahy © Humana Press Inc., Totowa, NJ

expansion. This, in turn, leads to mechanical compression of the emissary veins, thus inhibiting the drainage of blood, which results in an erection (9). Conversely, penile flaccidity results from the release of norepinephrine (NE) from sympathetic nerve terminals and contraction of smooth muscle tissue within the corpora. Corporeal smooth muscle tone is a critical determinant in the control of penile erections (10,11).

Blood flow to the penis is controlled by the autonomic erection center, the source of parasympathetic (S2-S4) and sympathetic (T12-L2) input to the pelvic plexus, as well as the cavernous nerves innervating the trabecular smooth muscle (11). Neural stimulation is transmitted through the Nervi erigentes (i.e., the pelvic autonomic fibers), which release three important neurotransmitters: (a) norepinephrine (sympathetic fibers); (b) acetylcholine (ACh; parasympathetic); and (c) nitric oxide (NO; nonadrenergic-non-cholinergic).

High levels of NO within the trabecular smooth muscle results in relaxation. Diffusion of NO through the smooth muscle membrane leads to the activation of guanylate cyclase, which produces cyclic guanosine monophosphate (cGMP). A biochemical cascade results in altered calcium and potassium ion channel permeability; a reduction in cytosolic calcium leads to smooth muscle relaxation and increased blood flow (12,13).

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